ArticleThe American journal of pathology1999
C6 produced by macrophages contributes to cardiac allograft rejection.
Article in The American journal of pathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 56 citations in OpenAlex.
- Genetically-engineered pigs as sources for clinical red blood cell transfusion: What pathobiological barriers need to be overcome?Blood reviews · 2019Review
- Article
- Molecules Great and Small: The Complement System.Clinical journal of the American Society of Nephrology : CJASN · 2015Review
- The changes of vaccinia related kinase 1 in grafted heart after rat heart transplantation.Journal of thoracic disease · 2014Article
- Immune cell-derived C3a and C5a costimulate human T cell alloimmunity.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2013Article
- Complement regulation of T cell immunity.Immunologic research · 2012Review
- B cells in cardiac transplants: from clinical questions to experimental models.Seminars in immunology · 2012Review
- Anti-complement component C5 mAb synergizes with CTLA4Ig to inhibit alloreactive T cells and prolong cardiac allograft survival in mice.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2011Article
- Complement regulation of T-cell alloimmunity.Current opinion in organ transplantation · 2011Review
- Platelets: versatile modifiers of innate and adaptive immune responses to transplants.Current opinion in organ transplantation · 2011Review
- Mechanisms involved in antibody- and complement-mediated allograft rejection.Immunologic research · 2010Review
- Mechanisms of complement activation, C4d deposition, and their contribution to the pathogenesis of antibody-mediated rejection.Transplantation reviews (Orlando, Fla.) · 2009Article
- The membrane attack complex (C5b-9) in liver cold ischemia and reperfusion injury.Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society · 2008Article
- The classical complement pathway in transplantation: unanticipated protective effects of C1q and role in inductive antibody therapy.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2008Article
- C4d deposition and cellular infiltrates as markers of acute rejection in rat models of orthotopic lung transplantation.Transplantation · 2008Article
- Critical role of effector macrophages in mediating CD4-dependent alloimmune injury of transplanted liver parenchymal cells.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Characterization of early and terminal complement proteins associated with polymorphonuclear leukocytes in vitro and in vivo after spinal cord injury.Journal of neuroinflammation · 2008Article
- New concepts of complement in allorecognition and graft rejection.Cellular immunology · 2007Review
- Cardiomyopathy is linked to complement activation.The American journal of pathology · 2002Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
The terminal components of complement C5b-C9 can cause significant injury to cardiac allografts. Using C6-deficient rats, we have found that the rejection of major histocompatibility (MHC) class I-incompatible PVG.R8 (RT1.A(a)B(u)) cardiac allografts by PVG.1U (RT1.A(u)B(u)) recipients is particularly dependent on C6. This model was selected to determine whether tissue injury results from C6 produced by macrophages, which are a conspicuous component of infiltrates in rejecting transplants. We demonstrated that high levels of C6 mRNA are expressed in isolated populations of macrophages. The relevance of macrophage-produced C6 to cardiac allograft injury was investigated by transplanting hearts from PVG. R8 (C6-) donors to PVG.1U (C6-) rats which had been reconstituted with bone marrow from PVG.1U (C6+) rats as the sole source of C6. Hearts grafted to hosts after C6 reconstitution by bone marrow transplantation underwent rejection characterized by deposition of IgG and complement on the vascular endothelium together with extensive intravascular aggregates of P-selectin-positive platelets. At the time of acute rejection, the cardiac allografts contained extensive perivascular and interstitial macrophage infiltrates. RT-PCR and in situ hybridization demonstrated high levels of C6 mRNA in the macrophage-laden transplants. C6 protein levels were also increased in the circulation during rejection. To determine the relative contribution to cardiac allograft rejection of the low levels of circulating C6 produced systemically by macrophages, C6 containing serum was passively transferred to PVG.1U (C6-) recipients of PVG.R8 (C6-) hearts. This reconstituted the C6 levels to about 3 to 6% of normal values, but failed to induce allograft rejection. In control PVG.1U (C6-) recipients that were reconstituted with bone marrow from PVG.1U (C6-) donors, C6 levels remained undetectable and PVG.R8 cardiac allografts were not rejected. These results indicate that C6 produced by macrophages can cause significant tissue damage.
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